NDLI: Glucose kinetics and exercise tolerance in mice lacking the GLUT4 glucose transporter

Content Provider	PubMed Central
Author	Fueger, Patrick T. Li, Candice Y. Ayala, Julio E. Shearer, Jane Bracy, Deanna P. Charron, Maureen J. Rottman, Jeffrey N. Wasserman, David H.
Copyright Year	2007
Abstract	The absence of GLUT4 severely impairs basal glucose uptake in vivo, but does not alter glucose homeostasis or circulating insulin. Glucose uptake in isolated contracting skeletal muscle (MGU) is also impaired by the absence of GLUT4, and onset of muscle fatigue is hastened. Whether the body can compensate and preserve glucose homeostasis during exercise, as it does in the basal state, is unknown. One aim was to test the effectiveness of glucoregulatory compensation for the absence of GLUT4 in vivo. The absence of GLUT4 was also used to further define the role of hexokinase (HK) II, which catalyses glucose phosphorylation after it is transported in the cell. HK II increases MGU during exercise, as well as exercise endurance. In the absence of GLUT4, HK II expression will not affect MGU. A second aim was to test whether, in the absence of GLUT4, HK II retains its ability to increase exercise endurance. Wild-type (WT), GLUT4 null (GLUT4−/−), and GLUT4 null overexpressing HK II (GLUT4−/−HKTg) mice were studied using a catheterized mouse model that allows blood sampling and isotope infusions during treadmill exercise. The impaired capacity of working muscle to take up glucose in GLUT4−/− is partially offset by an exaggerated increase in the glucagon: insulin ratio, increased liver glucose production, hyperglycaemia, and a greater capillary density in order to increase the delivery of glucose to the exercising muscle of GLUT4−/−. Hearts of GLUT4−/− also exhibited a compensatory increase in HK II expression and a paradoxical increase in glucose uptake. Exercise tolerance was reduced in GLUT4−/− compared to WT. As expected, MGU in GLUT4−/−HKTg was the same as in GLUT4−/−. However, HK II overexpression retained its ability to increase exercise endurance. In conclusion, unlike the basal state where glucose homeostasis is preserved, hyperglycaemia results during exercise in GLUT4−/− due to a robust stimulation of liver glucose release in the face of severe impairments in MGU. Finally, studies in GLUT4−/−HKTg show that HK II improves exercise tolerance, independent of its effects on MGU.
Related Links	http://dx.doi.org/10.1113/jphysiol.2007.132902
Starting Page	801
File Format	PDF
ISSN	14697793
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 2
Volume Number	582
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2007-07-15
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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